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Considering having an Austin plastic surgery procedure like Smartlipo? Then you’ll want to watch this quick video where staff members of renowned Austin plastic surgeon Dr. William Davis give you an overview of what you can expect.

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Immunomodulating effect of autohaemotherapy (a literature review). PMID 3534085 [PubMed indexed for MEDLINE]

J Hyg Epidemiol Microbiol Immunol. 1986;30(3):331-6.

Immunomodulating effect of autohaemotherapy (a literature review).
Klemparskaya NN, Shalnova GA, Ulanova AM, Kuzmina TD, Chuhrov AD.

Abstract
An analysis is presented of experimental and clinical data from different authors on the stimulating effect of autohaemotherapy with regard to the immunological reactivity of humans and animals as well as in vitro experiments with lymphocytes. Erythrolysate has been found to exert a more powerful effect than intact erythrocytes. The stimulating effect of autohaemotherapy on both irradiated and non-irradiated animals manifests itself in an increase in resistance to infection (increased LD50 in experimental infection), enhanced production of antibodies to microbial and tissue antigens and activated functioning of cell-mediated immune defence mechanisms. The favourable influences on radioresistance and the antitumour effect of authohaemotherapy are described. Induced desensitization plays an important part in the mechanism of action of autohaemotherapy. The administration of large doses of erythrocytes or of erythrolysate results in immunosuppression. Autohaemotherapy does not cause side effects and is feasible both on an in-and out-patient basis.

PMID: 3534085

[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/3534085

Autohemotherapy: an immunization with our own blood

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http://autohemoterapia.fortunecity.com/

http://www.geocities.ws/autohemoterapiabr/aht_english.htm

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Auto-hemotherapy PDF files in GOOGLE sites:

https://sites.google.com/site/autohemotherapy/

A clavicle fracture is a bone fracture in the clavicle, or collarbone. It is often caused by a fall onto an outstretched upper extremity, a fall onto a shoulder, or a direct blow to the clavicle. Many research projects are underway regarding the medical healing process of clavicle fractures.

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Debulking is the surgical removal of part of a malignant tumour which cannot be completely excised, so as to enhance the effectiveness of radiation or chemotherapy. It is used only in specific malignancies, as generally partial removal of a tumor is not considered a worthwhile intervention. Ovarian carcinoma and some types of brain tumor are debulked prior to commencing radio- or chemotherapy. It may also be used in the case of slow growth tumors to shift tumor cells from phase of cell cycle to replicative pool.

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Like in any other sector of health, aging come with its myths. These myths can be hurtful to senior citizens and their caretakers if mistaken for truths. Here are some common myths about aging that caregivers should be aware of.

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An amputation is the removal of an extremity or appendage from the body. Amputations in the upper extremity can occur as a result of trauma, or they can be performed in the treatment of congenital or acquired conditions. Although successful replantation represents a technical triumph to the surgeon, the patient's best interests should direct the treatment of amputations. The goals involved in the treatment of amputations of the upper extremity include the following : Preservation of functional length Durable coverage Preservation of useful sensibility Prevention of symptomatic neuromas Prevention of adjacent joint contractures Early return to work Early prosthetic fitting These goals apply differently to different levels of amputation. Treatment of amputations can be challenging and rewarding. It is imperative that the surgeon treat the patient with the ultimate goal of optimizing function and rehabilitation and not become absorbed in the enthusiasm of the technical challenge of the replantation, which could result in poorer outcome and greater financial cost due to lost wages, hospitalization, and therapy.

Tracheotomy is a surgical procedure which consists of making an incision on the anterior aspect of the neck and opening a direct airway through an incision in the trachea (windpipe). The resulting stoma (hole), or tracheostomy, can serve independently as an airway or as a site for a tracheostomy tube to be inserted; this tube allows a person to breathe without the use of his or her nose or mouth. Both surgical and percutaneous techniques are widely used in current surgical practice. It is among the oldest described procedures.

Fifth disease is a mild rash illness caused by parvovirus B19. This disease, also called erythema infectiosum, got its name because it was fifth in a list of historical classifications of common skin rash illnesses in children. It is more common in children than adults. A person usually gets sick with fifth disease within 4 to 14 days after getting infected with parvovirus B19.

Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo

Dilated cardiomyopathy is a disease of the heart muscle, usually starting in your heart's main pumping chamber (left ventricle). The ventricle stretches and thins (dilates) and can't pump blood as well as a healthy heart can. The term "cardiomyopathy" is a general term that refers to the abnormality of the heart muscle itself. Dilated cardiomyopathy might not cause symptoms, but for some people it can be life-threatening. A common cause of heart failure — the heart's inability to supply the body with enough blood — dilated cardiomyopathy can also contribute to irregular heartbeats (arrhythmias), blood clots or sudden death. The condition affects people of all ages, including infants and children, but is most common in men ages 20 to 60.

Friedreich's ataxia is an inherited disease that damages your nervous system. The damage affects your spinal cord and the nerves that control muscle movement in your arms and legs. Symptoms usually begin between the ages of 5 and 15. The main symptom is ataxia, which means trouble coordinating movements. Specific symptoms include Difficulty walking Muscle weakness Speech problems Involuntary eye movements Scoliosis (curving of the spine to one side) Heart palpitations, from the heart disease which can happen along with Friedreich's ataxia People with Friedreich's ataxia usually need a wheelchair 15 to 20 years after symptoms first appear. In severe cases, people become incapacitated. There is no cure. You can treat symptoms with medicines, braces, surgery, and physical therapy.

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection injury of the spinal cord, often in the cervical cord region. (See Presentation.) Patients with Brown-Séquard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrome. (See Etiology, Presentation, and Workup.) As an incomplete spinal cord syndrome, the clinical presentation of Brown-Séquard syndrome may range from mild to severe neurologic deficit. (See Presentation.) Brown-Séquard–plus syndrome The pure Brown-Séquard syndrome reflecting hemisection of the cord is not often observed. A clinical picture composed of fragments of the syndrome or of the hemisection syndrome plus additional symptoms and signs is more common. These less-pure forms of the disorder are often referred to as Brown-Séquard–plus syndrome.[1] Interruption of the lateral corticospinal tracts, the lateral spinal thalamic tract, and at times the posterior columns produces a picture of a spastic, weak leg with brisk reflexes and a strong leg with loss of pain and temperature sensation. Note that spasticity and hyperactive reflexes may not be present with an acute lesion.

A salivary gland stone -- also called salivary duct stone -- is a calcified structure that may form inside a salivary gland or duct. It can block the flow of saliva into the mouth. The majority of stones affect the submandibular glands located at the floor of the mouth. Less commonly, the stones affect the parotid glands, located on the inside of the cheeks, or the sublingual glands, which are under the tongue. Many people with the condition have multiple stones. Salivary Gland Stone Causes and Symptoms Salivary stones form when chemicals in the saliva accumulate in the duct or gland. They mostly contain calcium. The exact cause is not known. But factors contributing to less saliva production and/or thickened saliva may be risk factors for salivary stones. These factors include: dehydration, poor eating, and use of certain medications (such as antihistamines), blood pressure drugs, psychiatric drugs, and bladder control drugs. Trauma to the salivary glands may also raise the risk for salivary stones. The stones cause no symptoms as they form, but if they reach a size that blocks the duct, saliva backs up into the gland, causing pain and swelling. You may feel the pain off and on, and it may get progressively worse. Inflammation and infection within the affected gland may follow. Salivary Gland Stones Diagnosis and Treatments If you have symptoms of a salivary gland stone, your doctor will first check for stones with a physical exam. Sometimes tests may also be ordered, such as X-ray, CT scan, or ultrasound.